Trepopnea: A Comprehensive Review

 

Trepopnea: A Comprehensive Review for the Internist

Dr Neeraj Manikath , claude.ai

Abstract

Trepopnea, the preferential positional dyspnea relieved by lateral decubitus positioning, represents a unique clinical sign that often goes unrecognized in contemporary practice. This review examines the pathophysiology, differential diagnosis, clinical assessment, and management strategies for trepopnea, with emphasis on practical pearls for the postgraduate internist. Understanding this phenomenon can provide crucial diagnostic insights across multiple organ systems, from cardiac and pulmonary to neurological disorders.

Introduction

Trepopnea (from Greek trepo meaning "to turn" and pnea meaning "breath") describes dyspnea that occurs in one lateral decubitus position and is relieved by turning to the opposite side. While orthopnea and platypnea are well-recognized positional dyspneas in medical literature, trepopnea remains underappreciated despite its significant diagnostic implications. First systematically described in cardiac patients, trepopnea has since been associated with diverse pathologies affecting cardiopulmonary mechanics, ventilation-perfusion matching, and intracardiac shunting.

The recognition of trepopnea requires astute clinical observation, as patients may not spontaneously report this symptom. Many patients with trepopnea adapt their sleeping position unconsciously, sleeping exclusively on one side without recognizing this as pathological. The informed clinician must specifically inquire about positional dyspnea during history-taking.

Pathophysiology

The mechanisms underlying trepopnea are multifactorial and depend on the underlying pathology. Understanding these mechanisms is essential for accurate diagnosis and targeted management.

Gravitational Effects on Pulmonary Perfusion

In the lateral decubitus position, gravitational forces redistribute pulmonary blood flow preferentially to the dependent lung. Normal lungs accommodate this redistribution without difficulty. However, when significant unilateral lung disease exists, positioning the diseased lung in the dependent position creates ventilation-perfusion mismatch. The dependent diseased lung receives increased blood flow but cannot adequately oxygenate it, resulting in hypoxemia and dyspnea. Conversely, positioning the healthy lung dependently optimizes gas exchange.

Cardiac Mechanisms

In patients with unilateral intracardiac masses (atrial myxomas, thrombi, or tumors), positional changes can lead to mechanical obstruction of cardiac inflow or outflow tracts. When lying on the side of the mass, gravitational forces may cause the tumor to prolapse into the mitral or tricuspid valve orifice, obstructing flow and causing dyspnea. Platypnea-orthodeoxia syndrome, often associated with interatrial shunting, can manifest with trepopnea when the right-to-left shunt is position-dependent.

Mediastinal and Pleural Factors

Large unilateral pleural effusions create preferential dyspnea when the affected side is dependent due to compression atelectasis and reduced ventilation of the underlying lung. Mediastinal masses may cause positional airway compression or vascular obstruction. Pericardial disease can occasionally present with trepopnea through similar mechanisms.

Pulmonary Vascular Mechanisms

Unilateral pulmonary embolism or pulmonary artery hypoplasia can produce trepopnea through asymmetric perfusion patterns. Hepatopulmonary syndrome with preferential basilar arteriovenous shunting may manifest position-dependent hypoxemia, particularly when combined with anatomical asymmetries.

Clinical Conditions Associated with Trepopnea

Unilateral Lung Disease

Pneumonia and Lung Abscess: Unilateral pneumonia, particularly when extensive, classically produces trepopnea with relief when the healthy lung is positioned dependently. This phenomenon was historically termed "prefer to lie on the healthy side" and was recognized in pre-antibiotic era textbooks.

Unilateral Pleural Effusion: Large effusions cause trepopnea through compression of the underlying lung. Patients typically prefer lying on the unaffected side. However, small effusions rarely cause trepopnea, and bilateral effusions typically cause orthopnea rather than trepopnea.

Unilateral Pulmonary Fibrosis: Advanced unilateral fibrotic lung disease can produce trepopnea, though this is relatively uncommon given the typical bilateral nature of most interstitial lung diseases.

Post-Pneumonectomy: Patients post-pneumonectomy may develop trepopnea, particularly if complications such as bronchopleural fistula or empyema occur. These patients typically prefer lying on the operative (absent lung) side to optimize ventilation of the remaining lung.

Cardiac Pathology

Atrial Myxoma: Left atrial myxomas are the classic cardiac cause of trepopnea. These pedunculated tumors can obstruct the mitral valve orifice position-dependently, causing dyspnea, presyncope, or syncope. The direction of preferred positioning depends on tumor attachment site and mobility.

Intracardiac Thrombi: Similar to myxomas, mobile atrial or ventricular thrombi can cause positional symptoms. This is particularly relevant in patients with atrial fibrillation, dilated cardiomyopathy, or mechanical valves with inadequate anticoagulation.

Interatrial Septal Abnormalities: Patent foramen ovale or atrial septal defects with position-dependent right-to-left shunting can produce trepopnea with associated hypoxemia.

Vascular Causes

Unilateral Pulmonary Embolism: Significant unilateral pulmonary embolism can produce trepopnea through asymmetric perfusion patterns. This is more common with massive or submassive emboli affecting an entire lung.

Pulmonary Arteriovenous Malformations: When predominantly unilateral, these can cause position-dependent hypoxemia.

Other Causes

Mediastinal Masses: Large thymic tumors, lymphomas, or substernal goiters may cause positional airway or vascular compression.

Hemidiaphragm Paralysis: Unilateral diaphragmatic paralysis can occasionally produce trepopnea, with preference for lying on the paralyzed side to optimize function of the intact hemidiaphragm.

Obesity: Severe obesity, particularly when asymmetric, may contribute to positional dyspnea patterns.

Clinical Assessment

History Taking: The Key to Recognition

Pearl #1: Always ask specifically: "Do you feel more short of breath lying on one side versus the other?" or "When lying down, do you have a preferred side?" Patients often adapt unconsciously and won't volunteer this information.

Pearl #2: Inquire about orthopnea, platypnea, and paroxysmal nocturnal dyspnea to differentiate trepopnea from other positional dyspneas. Document the specific side that provokes symptoms.

Pearl #3: Ask about associated symptoms: presyncope suggests cardiac mass; pleuritic chest pain suggests pleural or parenchymal disease; hemoptysis raises concern for infection, malignancy, or pulmonary embolism.

Physical Examination

Physical examination should focus on identifying underlying cardiopulmonary pathology:

• Vital signs: Measure oxygen saturation in both lateral positions if trepopnea is suspected. A drop of ≥4% suggests significant physiological impact.

• Cardiac examination: Auscultate for murmurs in multiple positions. A "tumor plop" after S2 suggests atrial myxoma. Positional variation in murmur intensity supports position-dependent valvular obstruction.

• Pulmonary examination: Asymmetric breath sounds, dullness to percussion, or egophony suggests unilateral parenchymal or pleural disease.

• Observe patient positioning: Note if the patient spontaneously assumes a particular lateral position during the interview.

Oyster #1: Patients with trepopnea from atrial myxoma may have normal examination in supine position. Always auscultate in multiple positions, including lateral decubitus, when evaluating dyspnea of unclear etiology.

Diagnostic Approach

Initial Investigations:

• Chest radiograph (PA and lateral): Identifies unilateral infiltrates, effusions, masses, or cardiomegaly
• Electrocardiogram: Assesses for arrhythmias, particularly atrial fibrillation
• Complete blood count: Evaluates for infection, anemia
• Basic metabolic panel, brain natriuretic peptide

Advanced Imaging:

• Transthoracic echocardiography: Essential when cardiac etiology suspected. Perform with patient in multiple positions to identify mobile masses or position-dependent valvular obstruction.

• Computed tomography chest with contrast: Superior for evaluating pulmonary parenchyma, pleura, mediastinum, and pulmonary vasculature. CT angiography if pulmonary embolism suspected.

• Ventilation-perfusion scanning: Useful for suspected unilateral pulmonary embolism or pulmonary artery abnormalities.

Positional Pulse Oximetry Testing:

Hack #1: Perform systematic positional oxygen saturation monitoring. Measure SpO2 with patient supine, then in right and left lateral decubitus positions after 2-3 minutes in each position. Document the position, saturation, and patient's dyspnea severity (0-10 scale) in each position. This simple bedside test can be diagnostically illuminating and is often overlooked.

Management Strategies

Management of trepopnea is directed at the underlying cause:

Treatment of Underlying Conditions

Infectious/Inflammatory: Appropriate antimicrobials for pneumonia or lung abscess; drainage of pleural effusions or empyema; anti-inflammatory therapy for inflammatory conditions.

Cardiac: Surgical resection of cardiac tumors or mobile thrombi; anticoagulation for atrial fibrillation; closure of interatrial septal defects when appropriate; management of heart failure.

Pulmonary Vascular: Anticoagulation and thrombolysis for pulmonary embolism; embolization or surgery for arteriovenous malformations.

Neoplastic: Chemotherapy, radiation, or surgical resection for thoracic malignancies.

Symptomatic Management

Pearl #4: While addressing the underlying cause, educate patients about optimal positioning. Patients with unilateral lung disease should sleep with the healthy lung dependent. Elevate the head of bed for those with concurrent orthopnea.

Pearl #5: Supplemental oxygen may temporarily alleviate symptoms while definitive treatment is arranged, but should not delay diagnosis.

Hack #2: For hospitalized patients with trepopnea, clearly document the preferred position in the medical record and on the bedside communication board. This prevents well-intentioned staff from repeatedly repositioning patients into their symptomatic position.

Special Clinical Scenarios

The Post-Cardiac Surgery Patient

Oyster #2: New-onset trepopnea after cardiac surgery should prompt immediate evaluation for intracardiac thrombus, particularly in patients with mechanical valves or reduced left ventricular function. Don't attribute all post-operative dyspnea to expected surgical recovery.

The Patient with Chronic Trepopnea

Some patients develop chronic, stable trepopnea from irreversible conditions such as post-pneumonectomy state or severe unilateral pulmonary fibrosis. These patients benefit from:

• Patient education about optimal positioning
• Positional therapy devices (pillows, positioning aids)
• Pulmonary rehabilitation
• Supplemental oxygen if hypoxemic
• Treatment of comorbid conditions (heart failure, COPD)

Hack #3: Consider screening overnight oximetry or polysomnography in patients with chronic trepopnea, as they may develop position-dependent nocturnal hypoxemia requiring nocturnal oxygen therapy or positional therapy during sleep.

Trepopnea in Critical Care

In mechanically ventilated patients, recognition of trepopnea may guide optimal positioning for prone ventilation protocols or help identify asymmetric lung pathology requiring independent lung ventilation strategies.

Differential Diagnosis Pitfalls

Pearl #6: Not all positional dyspnea is trepopnea. Differentiate from:

• Orthopnea: Dyspnea when supine (typical of heart failure)
• Platypnea: Dyspnea when upright (hepatopulmonary syndrome, intracardiac shunts)
• Bendopnea: Dyspnea when bending forward (heart failure)
• Trepopnea vs. pleuritic pain: Patients may preferentially lie on one side due to chest wall or pleural pain rather than dyspnea. Careful history distinguishes these.

Oyster #3: Bilateral pleural effusions do not cause trepopnea; they cause orthopnea. If a patient with bilateral effusions reports trepopnea, look for asymmetry in effusion size or for an additional unilateral pathology.

Prognosis and Follow-up

The prognosis of trepopnea depends entirely on the underlying etiology. Reversible causes (pneumonia, pleural effusion, mobile cardiac thrombus) carry excellent prognosis with appropriate treatment. Irreversible conditions (post-pneumonectomy, severe unilateral fibrosis) require chronic management.

Pearl #7: Resolution of trepopnea serves as a useful clinical marker of treatment response. Systematically reassess positional symptoms during follow-up visits to gauge therapeutic efficacy.

Conclusion

Trepopnea represents a valuable clinical sign that, when recognized, can guide diagnostic evaluation and management of diverse cardiopulmonary pathology. The postgraduate internist must maintain high clinical suspicion for trepopnea, specifically inquire about positional dyspnea, and perform systematic positional assessment including pulse oximetry. Simple bedside evaluation can yield profound diagnostic insights. As Sir William Osler noted, "Listen to your patient; he is telling you the diagnosis"—but sometimes we must ask the right questions to hear the answer. In the case of trepopnea, asking specifically about lateral positioning preferences can unlock diagnostic mysteries that routine evaluation might miss.

Final Hack: Create a "positional dyspnea protocol" for your service: standardized questions about preferred positioning, systematic positional pulse oximetry, and documentation guidelines. This systematic approach will improve recognition of this underappreciated clinical sign.

Selected References

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